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β-咔啉衍生物DMCM与培养的小鼠神经元上抑制性氨基酸反应的相互作用。

The interaction of the beta-carboline derivative DMCM with inhibitory amino acid responses on cultured mouse neurones.

作者信息

Jensen M S, Lambert J D

出版信息

Neurosci Lett. 1983 Sep 30;40(2):175-9. doi: 10.1016/0304-3940(83)90298-7.

Abstract

Benzodiazepine (BZ) and GABA receptors are associated in the neuronal membrane. GABA responses are enhanced in the presence of BZs. The convulsant DMCM (methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate), like other beta-carbolines, binds with high affinity to BZ receptors. The effects of DMCM and of the BZ midazolam, on GABA responses, were studied in mouse cultured neurones using intracellular recording techniques. GABA responses were usually reduced by DMCM and potentiated by midazolam. This, with an occasional direct facilitatory effect on the membrane, is consistent with the convulsive action of DMCM.

摘要

苯二氮䓬(BZ)受体与γ-氨基丁酸(GABA)受体在神经元膜上相关联。在存在苯二氮䓬的情况下,GABA反应会增强。惊厥剂DMCM(6,7-二甲氧基-4-乙基-β-咔啉-3-羧酸甲酯)与其他β-咔啉一样,能高亲和力地结合到BZ受体上。利用细胞内记录技术,在小鼠培养神经元中研究了DMCM和BZ咪达唑仑对GABA反应的影响。DMCM通常会降低GABA反应,而咪达唑仑则会增强GABA反应。这一点,再加上偶尔对膜的直接促进作用,与DMCM的惊厥作用是一致的。

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